TargetRx Atlas

MRNA basic information

  • mRNA ID:ENST00000544301
  • Gene Name:VIM
  • mRNA database:Ensembl
  • mRNA expression :up-regulated
  • mRNA Method:RT-PCR
  • mRNA Pathway:NA
  • Evidence:predicted
  • (mRNA-drug)

Drug basic information

  • Drug ID:NA
  • Drug Name:NA
  • Drug Method:NA

Disease basic infommation

  • Disease:non-small cell lung cancer
  • Tissue:The human NSCLC A549

Other information

  • Title:IL-37 inhibits invasion and metastasis in non-small cell lung cancer by suppressing the IL-6/STAT3 signaling pathway.
  • Journal:Thorac Cancer
  • Published:2018
  • PubMed ID:29575809
  • Abstract:Background:IL-37 has been identified as a fundamental inhibitor of inflammatory and immunity responses. It plays a crucial protective role in several cancers, but its anti-tumor activity and the potential regulatory mechanism of IL-37 in non-small cell lung cancer (NSCLC) is largely unclear. Methods:Enzyme-linked immunosorbent assay was used to detect plasma IL-37 expression in NSCLC patients and healthy controls. The NSCLC cell line A549 was cultured with recombinant human IL-37 or recombinant human IL-6 protein. A549 invasion and metastasis were detected using Transwell invasion and scratch wound healing assays, respectively. Protein expression of STAT3, pSTAT3, E-cadherin, vimentin, and N-cadherin were detected using Western blotting, and messenger RNA expression of STAT3, E-cadherin, vimentin, and N-cadherin was assessed in each group using real time PCR. Results:IL-37 plasma expression was decreased in NSCLC patients, and the downregulation of IL-37 was correlated with tumor stage. In vitro, IL-37 inhibited invasion and migration in A549 cells, while IL-6 promoted invasion and migration in A549 cells. pSTAT3, vimentin, and N-cadherin expression was increased. E-cadherin expression was lower in the IL-6 group than in the control group; however, the opposite pattern was observed in the IL-37 + IL-6 group. Conclusion:Our results showed that IL-37 plays an inhibitory role in NSCLC progression, possibly by suppressing STAT3 activation and decreasing epithelial-to-mesenchymal transition by inhibiting IL-6 expression. IL-37 could serve as a potential novel tumor suppressor in NSCLC.